大黄素甲醚对胰腺癌SW1990细胞的杀伤作用及其机制

Mechanism and inhibitory effect of physcion on pancreatic cancer cell SW1990

目的观察大黄素甲醚对胰腺癌SW1990细胞增殖、细胞周期及凋亡的影响,并探讨其作用机制。方法 Western印迹检测不同浓度大黄素甲醚干预后PI3K/Akt信号通路蛋白水平,MTT检测不同浓度、时间下,大黄素甲醚对SW1990细胞增殖的影响。流式细胞术检测大黄素甲醚对SW1990周期及凋亡的影响。结果与NC组比较,Physcion组m TOR及p-Akt表达水平呈剂量依赖性下降,Akt表达呈剂量依赖性上升,其中5、50μmol/L组与NC组比较差异有统计学意义(P<0.05);Physcion组细胞存活率呈时间依赖性下降,在48、72、96h时,与NC组比较差异有统计学意义(P<0.05)。Physcion组SW1990存活率呈剂量依赖性下降,其中0.5、5、50μmol/L组与NC组比较差异有统计学意义(P<0.05);与NC组比较,Physcion组停留在G1、G2期细胞比例减少,S期细胞比例升高(P<0.05);Physcion组凋亡率高于NC组(P<0.01)。结论大黄素甲醚通过抑制Akt磷酸化,调控PI3K/Akt通路,降低胰腺癌细胞存活率,促进其凋亡。

Objective To observe the effect of physcion on proliferation and apoptosis of pancreatic cancer cell SW1990 and discuss the mechanism.Methods The PI3K-Akt-mTOR signaling pathway was detected by western blot;the proliferation of SW1990 interfered with different concentration of physcion at different time points was observed by MTT assay;the cell cycle and apoptosis affected by physcion was detected by flow cytometry.Results Compared with NC group,the expression of mTOR and p-Akt in physcion groups was dose-dependently decreased,while the expression of Akt was dose-dependently increased;there were significant differences at 5 μmol/L and 50μmol/L（P〈0.05）.The cell viability in physcion groups was decreased in a time-dependent or dose-dependent manner,the differences being significant at 48,72 and 96 h（P〈0.05） or 0.5,5 and 50 μmol/L（P〈0.05）.Physcion group has fewer cells staying in phase G1 and G2 and more cells staying in phase S than NC group（P〈0.05） with higher apoptosis rate（P〈0.01）.Conclusion Physcion decreases the cell viability of pancreatic cancer and promotes the apoptosis by inhibiting the phosphorylation of Akt and controlling the PI3K/Akt pathway.